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Steady state visual evoked potentials (SSVEPs)-based Brain-Computer interfaces (BCIs), as well as eyetracking devices, provide a pathway for re-establishing communication for people with severe disabilities. We fused these control techniques into a novel eyetracking/SSVEP hybrid system, which utilizes eye tracking for initial rough

Steady state visual evoked potentials (SSVEPs)-based Brain-Computer interfaces (BCIs), as well as eyetracking devices, provide a pathway for re-establishing communication for people with severe disabilities. We fused these control techniques into a novel eyetracking/SSVEP hybrid system, which utilizes eye tracking for initial rough selection and the SSVEP technology for fine target activation. Based on our previous studies, only four stimuli were used for the SSVEP aspect, granting sufficient control for most BCI users. As Eye tracking data is not used for activation of letters, false positives due to inappropriate dwell times are avoided. This novel approach combines the high speed of eye tracking systems and the high classification accuracies of low target SSVEP-based BCIs, leading to an optimal combination of both methods. We evaluated accuracy and speed of the proposed hybrid system with a 30-target spelling application implementing all three control approaches (pure eye tracking, SSVEP and the hybrid system) with 32 participants. Although the highest information transfer rates (ITRs) were achieved with pure eye tracking, a considerable amount of subjects was not able to gain sufficient control over the stand-alone eye-tracking device or the pure SSVEP system (78.13% and 75% of the participants reached reliable control, respectively). In this respect, the proposed hybrid was most universal (over 90% of users achieved reliable control), and outperformed the pure SSVEP system in terms of speed and user friendliness. The presented hybrid system might offer communication to a wider range of users in comparison to the standard techniques.
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Whole-brain networks derived from diffusion tensor imaging (DTI) data require the identification of seed and target regions of interest (ROIs) to assess connectivity patterns. This study investigated how initiating tracts from gray matter (GM) or white matter (WM) seed ROIs impacts (1) structural networks constructed from DTI data from healthy elderly (control) and individuals with Alzheimer’s disease (AD) and (2) between-group comparisons using these networks. DTI datasets were obtained from the Alzheimer’s disease Neuroimaging Initiative database. Deterministic tractography was used to build two whole-brain networks for each subject; one in which tracts were initiated from WM ROIs and another in which they were initiated from GM ROIs. With respect to the first goal, in both groups, WM-seeded networks had approximately 400 more connections and stronger connections (as measured by number of streamlines per connection) than GM-seeded networks, but shared 94% of the connections found in the GM-seed networks. With respect to the second goal, between-group comparisons revealed a stronger subnetwork (as measured by number of streamlines per connection) in controls compared to AD using both WM-seeded and GM-seeded networks. The comparison using WM-seeded networks produced a larger (i.e., a greater number of connections) and more significant subnetwork in controls versus AD. Global, local, and nodal efficiency were greater in controls compared to AD, and between-group comparisons of these measures using WM-seeded networks had larger effect sizes than those using GM-seeded networks. These findings affirm that seed location significantly affects the ability to detect between-group differences in structural networks.
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The neurological impact of Human Immunodeficiency Virus (HIV) on children includes loss of brain growth, motor abnormalities and cognitive dysfunction. Despite early antiretroviral treatment (ART) intervention to suppress viral load, neurological consequences of perinatal HIV-1 infection persist. Utilizing the pediatric simian immunodeficiency virus (SIV) infection model, we tested the hypothesis that early-life SIV infection depletes neuronal population in the hippocampus. A total of 22 ART-naïve infant rhesus macaques (Macaca mulatta) from previous studies were retrospectively analyzed. Infant macaques were either intravenously (IV) inoculated with highly virulent SIVmac251 at ~1 week of age and monitored for 6–10 weeks, or orally challenged with SIVmac251 from week 9 of age onwards with a monitoring period of 10–23 weeks post-infection (19–34 weeks of age), and SIV-uninfected controls were euthanized at 16–17 weeks of age. We have previously reported that the IV SIVmac251-infected neonatal macaques (Group 1) displayed a 42% neuronal reduction throughout the hippocampal cornu ammonis (CA) fields. The orally-infected infant macaques displayed a 75% neuronal reduction in the CA1 region compared to controls and 54% fewer neurons than IV SIV infants. The CA2 region showed a similar pattern, with a 67% reduction between orally-infected SIV subjects and controls and a 40% difference between IV-and orally-infected SIV groups. In the CA3 region, there were no significant differences between these groups, however both SIV-infected groups had significantly fewer pyramidal neurons than control subjects. There was no correlation between plasma viral load and neuronal populations in any of the CA fields. The loss of hippocampal neurons may contribute to the rapid neurocognitive decline associated with pediatric HIV infection. While each subfield showed vulnerability to SIV infection, the CA1 and CA2 subregions demonstrated a potentially enhanced vulnerability to pediatric SIV infection. These data underscore the need for early diagnosis and treatment, including therapeutics targeting the central nervous system (CNS).
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Hyperarousal is a 24-h state of elevated cognitive and physiological activation, and is a core feature of insomnia. The extent to which sleep quality is affected by stressful events—so-called sleep reactivity—is a vulnerability factor for developing insomnia. Given the increasing prevalence of insomnia

Hyperarousal is a 24-h state of elevated cognitive and physiological activation, and is a core feature of insomnia. The extent to which sleep quality is affected by stressful events—so-called sleep reactivity—is a vulnerability factor for developing insomnia. Given the increasing prevalence of insomnia with age, we aimed to investigate how hyperarousal and sleep reactivity were related to insomnia severity in different adult age groups. Data were derived from a large cohort study investigating the natural history of insomnia in a population-based sample (n = 1693). Baseline data of the Arousal Predisposition Scale (APS) and Ford Insomnia Response to Stress Test (FIRST) were examined across age and sleep/insomnia subgroups: 25–35 (n = 448), 35–45 (n = 528), and 45–55 year olds (n = 717); good sleepers (n = 931), individuals with insomnia symptoms (n = 450), and individuals with an insomnia syndrome (n = 312). Results from factorial analyses of variance (ANOVA) showed that APS scores decreased with increasing age, but increased with more severe sleep problems. FIRST scores were not significantly different across age groups, but showed the same strong increase as a function of sleep problem severity. The findings indicate that though arousal predisposition and sleep reactivity increase with more severe sleep problems, only arousal decreases with age. How arousing events affect an individual during daytime thus decreases with age, but how this arousal disrupts sleep is equivalent across different adult age groups. The main implication of these findings is that treatment of insomnia could be adapted for different age groups and take into consideration vulnerability factors such as hyperarousal and stress reactivity.
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The emergence of social neuroscience has significantly advanced our understanding of the relationship that exists between social processes and their neurobiological underpinnings. Social neuroscience research often involves the use of simple and static stimuli lacking many of the potentially important aspects of real

The emergence of social neuroscience has significantly advanced our understanding of the relationship that exists between social processes and their neurobiological underpinnings. Social neuroscience research often involves the use of simple and static stimuli lacking many of the potentially important aspects of real world activities and social interactions. Whilst this research has merit, there is a growing interest in the presentation of dynamic stimuli in a manner that allows researchers to assess the integrative processes carried out by perceivers over time. Herein, we discuss the potential of virtual reality for enhancing ecological validity while maintaining experimental control in social neuroscience research. Virtual reality is a technology that allows for the creation of fully interactive, three-dimensional computerized models of social situations that can be fully controlled by the experimenter. Furthermore, the introduction of interactive virtual characters—either driven by a human or by a computer—allows the researcher to test, in a systematic and independent manner, the effects of various social cues. We first introduce key technical features and concepts related to virtual reality. Next, we discuss the potential of this technology for enhancing social neuroscience protocols, drawing on illustrative experiments from the literature.
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Intensive sleep re-training is a promising new therapy for chronic insomnia. Therapy is completed over a 24-h period during a state of sleep deprivation. Improvements of sleep and daytime impairments are comparable to the use of stimulus control therapy but with the advantage

Intensive sleep re-training is a promising new therapy for chronic insomnia. Therapy is completed over a 24-h period during a state of sleep deprivation. Improvements of sleep and daytime impairments are comparable to the use of stimulus control therapy but with the advantage of a rapid reversal of the insomnia. The initial studies have been laboratory based and not readily accessible to the patient population. However, new smart phone technology, using a behavioral response to external stimuli as a measure of sleep/wake state instead of EEG determination of sleep, has made this new therapy readily available. Technological improvements are still being made allowing the therapy to provide further improvements in the effectiveness of Intensive Sleep Re-training.
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Schizophrenia patients are waiting for a treatment free of detrimental effects. Psychotic disorders are devastating mental illnesses associated with dysfunctional brain networks. Ongoing brain network gamma frequency (30–80 Hz) oscillations, naturally implicated in integrative function, are excessively amplified during hallucinations, in at-risk mental states for psychosis and first-episode psychosis. So, gamma oscillations represent a bioelectrical marker for cerebral network disorders with prognostic and therapeutic potential. They accompany sensorimotor and cognitive deficits already present in prodromal schizophrenia. Abnormally amplified gamma oscillations are reproduced in the corticothalamic systems of healthy humans and rodents after a single systemic administration, at a psychotomimetic dose, of the glutamate N-methyl-d-aspartate receptor antagonist ketamine. These translational ketamine models of prodromal schizophrenia are thus promising to work out a preventive noninvasive treatment against first-episode psychosis and chronic schizophrenia. In the present essay, transcranial electric stimulation (TES) is considered an appropriate preventive therapeutic modality because it can influence cognitive performance and neural oscillations. Here, I highlight clinical and experimental findings showing that, together, the corticothalamic pathway, the thalamus, and the glutamatergic synaptic transmission form an etiopathophysiological backbone for schizophrenia and represent a potential therapeutic target for preventive TES of dysfunctional brain networks in at-risk mental state patients against psychotic disorders.
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The central nervous system (CNS) is a very challenging HIV-1 sanctuary, in which HIV-1 replication is established early on during acute infection and can persist despite potent antiretroviral treatments. HIV-1 infected macrophages play a pivotal role acting as vehicles for HIV-1 to spread

The central nervous system (CNS) is a very challenging HIV-1 sanctuary, in which HIV-1 replication is established early on during acute infection and can persist despite potent antiretroviral treatments. HIV-1 infected macrophages play a pivotal role acting as vehicles for HIV-1 to spread into the brain, and can be the major contributor of an early compartmentalization. HIV-1 infection in CNS may lead to a broad spectrum of neurological syndromes, such as dementia, mild neurocognitive disorders, and asymptomatic impairment. These clinical manifestations are caused by the release of neurotoxins from infected cells (mainly macrophages), and also by several HIV-1 proteins, able to activate cell-signaling involved in the control of cellular survival and apoptosis. This review is aimed at highlighting the virological aspects associated with the onset of neurocognitive disorders and at addressing the novel therapeutic approaches to stop HIV-1 replication in this critical sanctuary.
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A subset of patients with a demyelinating disease suffer from concurrent cervical spondylotic myelopathy, both of which evince similar symptomatology. Differentiating the cause of these symptoms is challenging, and little research has been done on patients with coexisting diseases. This review explores the

A subset of patients with a demyelinating disease suffer from concurrent cervical spondylotic myelopathy, both of which evince similar symptomatology. Differentiating the cause of these symptoms is challenging, and little research has been done on patients with coexisting diseases. This review explores the current literature on the appropriate surgical management of patients with concurrent multiple sclerosis (MS) and cervical spondylotic myelopathy (CSM), and those with both Parkinson’s disease (PD) and CSM. MS and CSM patients may benefit from surgery to reduce pain and radiculopathy. Surgical management in PD and CSM patients has shown minimal quality-of-life improvement. Future studies are needed to better characterize demyelinating disease patients with concurrent disease and to determine ideal medical or surgical treatment.
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In recent years, two separate research streams have focused on information sharing between the medial prefrontal cortex (mPFC) and hippocampus (HC). Research into spatial working memory has shown that successful execution of many types of behaviors requires synchronous activity in the theta range

In recent years, two separate research streams have focused on information sharing between the medial prefrontal cortex (mPFC) and hippocampus (HC). Research into spatial working memory has shown that successful execution of many types of behaviors requires synchronous activity in the theta range between the mPFC and HC, whereas studies of memory consolidation have shown that shifts in area dependency may be temporally modulated. While the nature of information that is being communicated is still unclear, spatial working memory and remote memory recall is reliant on interactions between these two areas. This review will present recent evidence that shows that these two processes are not as separate as they first appeared. We will also present a novel conceptualization of the nature of the medial prefrontal representation and how this might help explain this area’s role in spatial working memory and remote memory recall.
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Diverse ‘-omics’ technologies permit the comprehensive quantitative profiling of a variety of biological molecules. Comparative ‘-omics’ analyses, such as transcriptomics and proteomics, are powerful and useful tools for unraveling the molecular pathomechanisms of various diseases. As enhanced oxidative stress has been demonstrated in

Diverse ‘-omics’ technologies permit the comprehensive quantitative profiling of a variety of biological molecules. Comparative ‘-omics’ analyses, such as transcriptomics and proteomics, are powerful and useful tools for unraveling the molecular pathomechanisms of various diseases. As enhanced oxidative stress has been demonstrated in humans and mice with Down syndrome (DS), a redox proteomic analysis is useful for understanding how enhanced oxidative stress aggravates the state of individuals with oxidative stress-related disorders. In this review, ‘-omics’ analyses in humans with DS and mouse models of DS are summarized, and the molecular dissection of this syndrome is discussed.
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Identifying, recruiting, and enrolling persons in clinical trials of dementia treatments is extremely difficult. One approach to first-wave screening of potential participants is the use of online assessment tools. Initial studies using the Dementia Risk Assessment (DRA)—which includes a previously validated recognition memory

Identifying, recruiting, and enrolling persons in clinical trials of dementia treatments is extremely difficult. One approach to first-wave screening of potential participants is the use of online assessment tools. Initial studies using the Dementia Risk Assessment (DRA)—which includes a previously validated recognition memory test—support the use of this self-administered assessment to identify individuals with “suspected MCI” or “suspected dementia.” In this study, we identified between 71 and 622 persons with suspected dementia and between 128 and 1653 persons with suspected mild cognitive impairment (depending on specific criteria) over the course of 22 months. Assessment tools that can inexpensively and easily identify individuals with higher than average risk for cognitive impairment can facilitate recruitment for large-scale clinical trials for dementia treatments.
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